The Incretins and β-Cell Health: Contrasting Glucose-Dependent Insulinotropic Polypeptide and Glucagon-Like Peptide-1 as a Path to Understand Islet Function in Diabetes  Lene Jessen, David D'Alessio  Gastroenterology  Volume 137, Issue 6, Pages 1891-1894 (December 2009) DOI: 10.1053/j.gastro.2009.10.013 Copyright © 2009 AGA Institute Terms and Conditions

Figure 1 Incretin actions on β-cells and plausible sites of differential effects. Although there is considerable overlap between pathways, GLP-1r activation may up-regulate IRS-2 expression through transactivation of the EGF receptor, resulting in more potent cytoprotective actions on β-cells. Other mechanisms could also mediate the differential effects of the incretins on β-cell functions. Akt/PKB, Akt-protein kinase B; cAMP, cyclic adenosine monophosphate; CREB, cAMP response element-binding protein; EGF, epidermal growth factor; Epac, guanine nucleotide exchange factor; ER, endoplasmic reticulum; Foxo1, forkhead box O1; IRS-2, insulin receptor substrate-2; MAPK, mitogen-activated protein kinase; NFAT, nuclear factor of activated T cells; NF-κB, nuclear factor-κ B; PDX-1, pancreas duodenum homeobox 1; PI-3K, phosphatidylinositol 3-kinase; PKA, protein kinase A; PKC, protein kinase C; VDCC, voltage-dependent calcium channels. Gastroenterology 2009 137, 1891-1894DOI: (10.1053/j.gastro.2009.10.013) Copyright © 2009 AGA Institute Terms and Conditions